doi:10.1100/2012/791460
The
cientific
WorldJOURNAL
Clinical Study
Higher
P-Wave Dispersion in Migraine Patients with
Higher Number of Attacks
A. Koc¸er,
1M. Eryılmaz,
2H. Tutkan,
3N. Ercan,
2and Z. S. K¨
uc¸¨
ukbayrak
41Neurology Department, Medical Faculty, Bezmialem Vakif University, Istanbul, Turkey 2Neurology Department, Medical Faculty, D¨uzce University, D¨uzce, Turkey
3Neurology Department, Sakarya State Hospital, Sakarya, Turkey 4Physiology Department, Medical Faculty, D¨uzce University, D¨uzce, Turkey
Correspondence should be addressed to A. Koc¸er,abdulkadirkocer@yahoo.com
Received 30 October 2011; Accepted 29 November 2011 Academic Editor: Ahmet Baydin
Copyright © 2012 A. Koc¸er et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Objective and Aim. An imbalance of the sympathetic system may explain many of the clinical manifestations of the migraine. We aimed to evaluateP-waves as a reveal of sympathetic system function in migraine patients and healthy controls. Materials and Methods. Thirty-five episodic type of migraine patients (complained of migraine during 5 years or more, BMI< 30 kg/m2) and 30
controls were included in our study. We measuredP-wave durations (minimum, maximum, and dispersion) from 12-lead ECG recording during pain-free periods. ECGs were transferred to a personal computer via a scanner and then used for magnification of x400 by Adobe Photoshop software. Results.P-wave durations were found to be similar between migraine patients and controls. AlthoughP WD (P-wave dispersion) was similar, the mean value was higher in migraine subjects. P WD was positively correlated withP max (P < 0.01). Attacks number per month and male gender were the factors related to the P WD (P < 0.01). Conclusions. Many previous studies suggested that increased sympathetic activity may cause an increase inP WD. We found that P WD of migraine patients was higher than controls, andP WD was related to attacks number per month and male gender. Further studies are needed to explain the chronic effects of migraine.
1. Introduction
It is widely accepted that symptoms of migraine are related to the involvement of the autonomic nervous system, and dysfunction may affect atrial and ventricular repolarization. The sympathetic nervous system is known to play an important role in the genesis of ventricular arrhythmias [1].
QT interval changes andP-wave changes may be predictors
of atrial and ventricular arrhythmias. The most significant one is prolonged QT interval, which is a predictor of
ventricular arrhythmias [2]. In addition,P-wave dispersion
which is a predictor of atrial fibrillation (AF) is defined
as the difference between maximum and minimum P-wave
duration and has been associated with inhomogeneous and
discontinuous propagation of sinus impulses [3, 4]. It has
been shown that increased sympathetic activity caused a
significant elevation in P-wave dispersion [5]. It has also
been reported that there was an association between the
autonomic nervous system and atrial fibrillation [6,7].
Although the previous reports reflected atrial and
ven-tricular repolarization abnormalities that were affected by
disturbed ANS (sympathetic and/or parasympathetic ner-vous system dysfunction) during migraine attacks, the asso-ciation between atrial fibrillation and migraine is limited to case reports only [8–12]. Duru et al. reported that maximum P-wave duration (P max) and P-wave disperson (P WD) were found higher during migraine attacks than during
pain-free periods [13]. However,P WD was not reported during
pain-free period which might be a shower of damage related to attacks until now in comparison to healthy controls. In this study, we tried to find whether the patients with migraine may go under the risk of atrial and ventricular arrhythmias
or not. For this reason, we undertook evaluation ofP-wave
2 The Scientific World Journal
Table 1: Sociodemographical and clinical variables andP-wave durations in comparison.
Variable Migraine group (n=35) Controls (n=30) P value
Age (year) 34.60±7.54 35.87±6.97 0.48
Gender 0.25
Male 6 9
Female 29 21
Number of the patients
with aura 14
without aura 21
Duration of migraine (hour) 22.43±22.85 (range: 3.0–72.0) Attack number per month 3.37±1.63 (range: 2.0–8.0)
VAS score 7.63±2.11 (range: 4.0–10.0)
P min value (ms) 41.81±8.02 42.36±8.07 0.78
P max value (ms) 95.97±12.89 91.21±10.05 0.11
P WD value (ms) 54.55±13.44 50.40±11.63 0.19
with well-defined migraine during headache-free period and compared to normal healthy controls.
2. Methods
Thirty-five episodic type of migraine patients (complained of
migraine during 5 years or more, BMI< 30 kg/m2), and age
and sex-matched 30 healthy controls were included in our study.
The diagnosis of migraine was made using criteria of the International Headache Society [14]. Thirty-five subjects with migraine were evaluated during the pain-free period; 14 with migraine with aura (MWA) and 21 with migraine without aura (MWOA). We confined the study to women aged 20 to 45 years who had suffered from migraine for more than 1 year and had at least one migraine attack per month. The presence of other pain syndromes (e.g., chronic low back pain or chronic tension-type headache), systemic disease
(e.g., diabetes mellitus), and disorders that could affect the
autonomic nervous system were exclusionary. Except for mild analgesics, all drugs were withdrawn 5 days before the
testing, and no drug, including caffeine, or cigarettes, was
allowed on the day of testing. The control group (n = l6)
consisted of age and sex-matched persons who were free of migraine, other chronic pain syndromes, systemic diseases,
or disorders that could affect the autonomic nervous system.
These subjects were not on any medication. The study protocol was approved by the Institutional Review Board.
Autonomic tests were performed in the headache-free period. None of the subjects reported headache for at least 72 h before and after testing. Subjects were instructed to abstain from caffeine-containing beverages and, in the adolescents, from nicotine and alcohol for at least 24 h before the test. The examinations took place between 14.00 h and 17.00 h to avoid diurnal variation and were performed in
a warm room (24◦C). The subjects were asked to lie down
and not to move during recording. The ECG recording
was performed. Heart rate, P max and minimum P-wave
duration (P min), and P WDwere measured from 12-lead
ECG recording during pain-free periods. The difference
between the maximum and minimumP-wave duration was
defined as P WD. ECGs were transferred to a personal
computer via a scanner and then used for magnification of x400 by Adobe Photoshop software.
Intra- and interobserver coefficients of variation
(stan-dard deviation [SD] of differences between 2 observations
divided by the mean value and expressed in percent) were
found as 3.7% and 3.8% forP-wave dispersion. Intra and
interobserver coefficients of variation were found to be
less than 5%. All data were presented as mean value ±
SD. Comparison of clinical variables between 2 groups was performed with paired Student t-test for numeric variables
and chi-square test for categorical data. AP value < 0.05 was
considered to be statistically significant. The SPSS version 11.0 package was used in statistical analysis.
3. Results
Sociodemographical and clinical findings andP-wave values
were summarized inTable 1. Ten patients were using
Trip-tans, 10 patients were using anti-inflammatory or analgesic
agents, and 15 patients were using combinations.P min was
found to be similar between migraine patients and controls.
AlthoughP WD and P max values of migraine patients were
similar in migraine patients and healthy controls, the mean
values were higher in migraine subjects as seen inTable 1.P
WD was positively correlated withP max (P < 0.001). On the
other hand, attacks number per month (P < 0.001) and male
gender (P =0.03) were the factors related to the P WD. In
addition,P max was positively correlated with age (P < 0.05).
VAS score was higher in females (P=0.02). The presence of
aura did not affect P value.
4. Discussion
Aura symptoms, gastrointestinal symptoms, and photosen-sitivity or phonosenphotosen-sitivity may be an imbalance of the
In addition, supporting sympathetic dysfunction, the systolic blood pressure overshoot during the Valsalva maneuver was found to be decreased in migraineurs with aura [15]. Dysfunction of the ANS may affect atrial and ventricular repolarization. For example, increased sympathetic activity causes increased heart rate. Therefore, disrupted autonomic innervation of the heart and coronary arteries in patients with migraine may result in possible electrocardiographic (ECG) abnormalities during headache. Some case-control studies of cardiovascular function reported both sympathetic hyperfunction [16–18] and sympathetic hypofunction [19] even using single-lead ECG monitoring during migraine compared with a pain-free period.
Reduced parasympathetic and increased sympathetic nervous system (SNS) activity can lower the threshold for atrial fibrillation. Some previous studies have reported the
association between the ANS and atrial fibrillation [20,21].
But we have limited information on the association between atrial fibrillation and migraine. Duru et al. have shown that the migraine attacks were associated with increased QTc
andP-wave dispersion compared with pain-free periods in
a recent paper. Then, they concluded that patients with migraine during attacks were associated with increased QTc
and P-wave dispersion because of a disrupted autonomic
nervous system in migraine patients [13]. However,P-wave
dispersion was not reported during pain-free period which might be a shower of damage related to attacks until now. In this study, we tried to find whether the patients with migraine may be under the risk of atrial and ventricular arrhythmias or not. For this reason, we undertook evaluation
of P-wave dispersion as a sign of autonomic dysfunction
in patients with well-defined migraine during headache-free period and compared to normal healthy controls. In
our study, we found that P max and P min were similar
between migraine patients and controls. Similarly, Aygun et al. reported that ECG abnormalities particularly PR and corrected QT (QTc) interval lengthening often were present during a migraine attack, and these abnormalities would be absent or less prominent during pain-free intervals [22]. Duru et al. also found that ECG abnormalities including P-wave dispersion were more prominent during migraine attack [13]. In addition to this previous knowledges we found
that the mean value ofP WD was higher in migraine subjects,
andP WD was positively correlated with P max.
In conclusion, we believe that increased sympathetic
activity may cause significant increase inP WD of migraine
patients. The attacks number per month and male gender are
the factors affecting the P WD, so the patients with higher
numbers of attack may go under the risk of autonomic-dysfunction-related problems in the future.
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4 The Scientific World Journal
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